Kisspeptin 10 (rat)

Immature rat seminal vesicles show histomorphological and ultrastructural alterations following treatment with kisspeptin-10.[Pubmed:22404961]

Reprod Biol Endocrinol. 2012 Mar 10;10:18.

BACKGROUND: Degenerative effects of critical regulators of reproduction, the kisspeptin peptides, on cellular aspects of sexually immature male gonads are known but similar information on accessory sex glands remain elusive. METHODS: Prepubertal laboratory rats were injected kisspeptin-10 at three different dosage concentrations (10 pg, 1 ng and 1 microgram) for a period of continuous 12 days at the rate of two doses per day. Control rats were maintained in parallel. The day following the end of the experimental period, seminal vesicles were removed and processed for light and electron microscopic examination using the standard methods. DNA damage was estimated by DNA ladder assay and DNA fragmentation assay. RESULTS: The results demonstrated cellular degeneration. Epithelial cell height of seminal vesicles decreased significantly at all doses (P < 0.05). Marked decrease in epithelial folds was readily noticeable, while the lumen was dilated. Ultrastructural changes were characterized by dilatation of endoplasmic reticulum and Golgi complex, heterochromatization of nuclei, invagination of nuclear membranes and a decreased number of secretory granules. Percent DNA damage to the seminal vesicle was 19.54 +/- 1.98, 38.06 +/- 2.09 and 58.18 +/- 2.59 at 10 pg, 1 ng and 1 microgram doses respectively. CONCLUSION: The study reveals that continuous administration of kisspeptin does not lead to an early maturation but instead severe degeneration of sexually immature seminal vesicles.

Kisspeptin-10 potentiates miniature excitatory postsynaptic currents in the rat supraoptic nucleus.[Pubmed:25130664]

Brain Res. 2014 Oct 2;1583:45-54.

Kisspeptin is the natural ligand of the G protein-coupled receptor -54 and plays a major role in gonadotropin-releasing hormone secretion in the hypothalamus. Kisspeptin-10 is an endogenous derivative of kisspeptin and has 10 -amino acids. Previous studies have demonstrated that central administration of kisspeptin-10 stimulates the secretion of arginine vasopressin (AVP) in male rats. We examined the effects of kisspeptin-10 on- excitatory synaptic inputs to magnocellular neurosecretory cells (MNCs) including AVP neurons in the supraoptic nucleus (SON) by obtaining in vitro whole-cell patch-clamp recordings from slice preparations of the rat brain. The application of kisspeptin-10 (100 nM-1 muM) significantly increased the frequency of miniature excitatory postsynaptic currents (mEPSCs) in a dose-related manner without affecting the amplitude. The kisspeptin-10-induced potentiation of the mEPSCs was significantly attenuated by previous exposure to the kisspeptin receptor antagonist kisspeptin-234 (100 nM) and to the protein kinase C inhibitor bisindolylmaleimide I (20 nM). These results suggest that kisspeptin-10 participates in the regulation of synaptic inputs to the MNCs in the SON by interacting with the kisspeptin receptor.

Kisspeptin-10 induces dose dependent degeneration in prepubertal rat prostate gland.[Pubmed:23129449]

Prostate. 2013 May;73(7):690-9.

BACKGROUND: Kisspeptin peptides mediate their actions through the GnRH loop system. How kisspeptins affect prostate gland in prepubertal male mammals remains elusive. METHODS: To address this kisspeptin was administered as subchronic (12 days) twice daily i.p. dose at three different dosage regimens: 10 pg, 1 ng and 1 microg, to prepubertal male Sprague-Dawley rats (PND 35). Control rats were maintained in parallel. At the end of the experiment prostate gland was dissected out and processed for light and electron microscopy. DNA damage was also estimated by DNA ladder assay and DNA fragmentation assay. RESULTS: Prostate weights decreased significantly (P < 0.05) at 1 microg treatment dose of kisspeptin. The epithelial height of secretory acini of prostate decreased at 10 pg (P < 0.05), 1 ng, and 1 microg doses (P < 0.001). Histomorphology and ultrastructure demonstrated, decrease in epithelial cell height, epithelial folding and dilatation of the organelles with kisspeptin treatment. Percent DNA damage to the prostatic tissue was 20.74 +/- 2.18, 43.60 +/- 2.39, and 58.18 +/- 2.59 at 10 pg, 1 ng and 1 microg doses, respectively. CONCLUSION: The study reveals that continuous administration of kisspeptin does not lead to an early maturation but instead severe degeneration of prepubertal prostate gland. Wiley Periodicals, Inc.

Kisspeptin-10 inhibits proliferation and regulates lipolysis and lipogenesis processes in 3T3-L1 cells and isolated rat adipocytes.[Pubmed:28194651]

Endocrine. 2017 Apr;56(1):54-64.

INTRODUCTION: Kisspeptin, which is encoded by the KISS1 gene and acts via GPR54, plays a role in the regulation of reproductive functions. Expression of KISS1 and GRPR54 has been found in peripheral tissues, including adipose tissue, and was shown to be influenced by metabolic status. PURPOSE: We hypothesized that kisspeptin could be involved in regulation of lipid metabolism in the mouse 3T3-L1 cell line and in isolated rat adipocytes. METHODS: First, we characterized expression profiles of KISS1 and GPR54 mRNA and proteins in adipose cells isolated from male rats. Secondly, we studied the effects of kisspeptin-10 on cell proliferation and survival in 3T3-L1 cells. Thirdly, we assessed the rapid action of kisspeptin-10 on lipid metabolism and glucose uptake using 3T3-L1 cells and rat primary adipocytes. Finally, we examined the effects of kisspeptin-10 on the secretion of leptin and adiponectin in rat adipocytes. RESULTS: We have found that: (1) KISS1 and GPR54 were expressed in mouse 3T3-L1 cells and isolated rat adipocytes; (2) kisspeptin-10: (i) inhibited cell proliferation, viability and adipogenesis in 3T3-L1 and decreased expression of PPAR-gamma and CEBPbeta-genes, which are involved in the differentiation processes and adipogenesis; (ii) increased lipolysis in 3T3-L1 cells and rat adipocytes by enhancing expression of periliphin and hormone-sensitive lipase; (iii) modulated glucose uptake and lipogenesis; (iv) stimulated leptin and decreased adiponectin secretion from rat adipocytes. CONCLUSION: Kisspeptin-10 could play a role in the regulation of lipid metabolism in mouse 3T3-L1 cells and rat adipocytes.

Developmental and hormonally regulated messenger ribonucleic acid expression of KiSS-1 and its putative receptor, GPR54, in rat hypothalamus and potent luteinizing hormone-releasing activity of KiSS-1 peptide.[Pubmed:15242985]

Endocrinology. 2004 Oct;145(10):4565-74.

The gonadotropic axis is centrally controlled by a complex regulatory network of excitatory and inhibitory signals that is activated at puberty. Recently, loss of function mutations of the gene encoding G protein-coupled receptor 54 (GPR54), the putative receptor for the KiSS-1-derived peptide metastin, have been associated with lack of puberty onset and hypogonadotropic hypogonadism. Yet the pattern of expression and functional role of the KiSS-1/GPR54 system in the rat hypothalamus remain unexplored to date. In the present work, expression analyses of KiSS-1 and GPR54 genes were conducted in different physiological and experimental settings, and the effects of central administration of KiSS-1 peptide on LH release were assessed in vivo. Persistent expression of KiSS-1 and GPR54 mRNAs was detected in rat hypothalamus throughout postnatal development, with maximum expression levels at puberty in both male and female rats. Hypothalamic expression of KiSS-1 and GPR54 genes changed throughout the estrous cycle and was significantly increased after gonadectomy, a rise that was prevented by sex steroid replacement both in males and females. Moreover, hypothalamic expression of the KiSS-1 gene was sensitive to neonatal imprinting by estrogen. From a functional standpoint, intracerebroventricular administration of KiSS-1 peptide induced a dramatic increase in serum LH levels in prepubertal male and female rats as well as in adult animals. In conclusion, we provide novel evidence of the developmental and hormonally regulated expression of KiSS-1 and GPR54 mRNAs in rat hypothalamus and the ability of KiSS-1 peptide to potently stimulate LH secretion in vivo. Our current data support the contention that the hypothalamic KiSS-1/GPR54 system is a pivotal factor in central regulation of the gonadotropic axis at puberty and in adulthood.

Identification and characterization of mouse metastasis-suppressor KiSS1 and its G-protein-coupled receptor.[Pubmed:12359743]

Cancer Res. 2002 Oct 1;62(19):5399-404.

G-protein-coupled receptors receive many different signals to activate different functions such as cellgrowth, proliferation, and migration. KiSS1 is a metastasis suppressor gene that has been shown to inhibit metastasis of human melanomas and breast carcinomas. The human KiSS1 gene encodes a COOH-terminally amidated active peptide, and this peptide is the ligand of a novel G-protein-coupled receptor. However, the mechanism of the antimetastatic actions of KiSS1 and its G-protein-coupled receptor has not been elucidated. In this study, we identified the mouse homologues of the KiSS1 peptide and its G-protein-coupled receptor and characterized the signaling pathways mediated by the activation of the KiSS1 receptor. Although human and mouse KiSS1 proteins share relatively low overall homology (52%), the active peptides (10-amino-acid residues) are highly conserved between mouse and human KiSS1 proteins, varying by only one conserved amino acid [Tyr (Y) to Phe (F)]. Activation of the receptor by KiSS1 peptide leads to the activation of G-protein-activated phospholipase C (PLC-beta), which suggests direct coupling of the KiSS1 peptide to the Galphaq-mediate PLC-Ca2+ signaling pathway. Furthermore, activation of the KiSS1 receptor inhibits cell proliferation and cell migration, key characteristics of tumor metastasis.

Kisspeptin-10, rat is a potent vasoconstrictor and inhibitor of angiogenesis. Kisspeptin-10, rat is a ligand for the rodent kisspeptin receptor (KISS1, GPR54). Kisspeptin-10 reduces Methotrexate-induced reproductive toxicity as a potential antioxidant compound.

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